The pseudogene legumain (LGMN) has been reported to regulate cancer cell biology. However, the role of LGMN in thyroid carcinoma remains unknown. Herein, Cell Counting Kit 8 and Transwell assays were performed to evaluate cellular proliferation and invasion capacity, respectively. In addition, a tube formation assay was performed to assess HUVEC angiogenesis. The results showed that LGMN depletion attenuated cellular proliferation, invasion and tube formation ability, and that LGMN expression was dysregulated in thyroid carcinoma tumors. Furthermore, patients with high LGMN expression levels exhibited a lower overall survival rate than those with low expression levels. LGMN and microRNA (miR)-495 modulated the expression levels of autophagy-related gene 3 (ATG3) and p62. Finally, ATG3 overexpression rescued the LGMN-regulated thyroid carcinoma phenotype. In conclusion, LGMN was found to promote thyroid carcinoma progression via the miR-495/autophagy axis, thus providing novel insights for understanding the pathogenesis of thyroid carcinoma.
Keywords: autophagy; legumain; microRNA-495; thyroid carcinoma.
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